Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

cardioresp > Sem2 > Flashcards

Sem2 Flashcards

1
Q

APO signs/symptoms - history

A

SOB, orthopnoea/bendopnoea, paroxysmal nocturnal dyspnoea, cough, anxiety, (chest pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

APO signs and symptoms - examination

A

Tachypnoea, course crackles, (wheeze), diaphoresis, tachycardia, hypertension, leg swelling/peripheral oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

APO signs and symptoms - investigation

A

Decreased SpO2, chest x-ray/POCUS showing fluid, ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

APO principles of treatment

A
  1. Symptomatic relief/reassurance
  2. Improve oxygenation
  3. Maintain cardiac output and perfusion of vital organs
  4. Reduce preload and after load
  5. Reduce excess extracellular fluid
  6. Identify and fix underlying cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

APO steps

A
  1. Inciting event e.g. AMI
  2. Decreased LV function
  3. Compensate by increasing stretch
  4. Pump failure so can’t overcome after load
  5. Back flow of blood into pulmonary circuit
  6. Increased hydrostatic pressure (more than oncotic) - lymphatic system can’t compensate
  7. Fluid in interstitial space increases membrane thickness - Fick’s law (sub clinical APO)
  8. Surfactant washed away
  9. Alveoli collapse decreasing surface area for gas exchange - Fick’s law
  10. Hypoxia/hypoxaemia causing SOB (clinical APO)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Shock definition

A

A state of cellular and tissue hypoxia due to reduced oxygen delivery and/or increased oxygen consumption and/or inadequate oxygen utilisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pre-shock/compensated shock characteristics

A

Compensatory mechanisms activated in response to diminished tissue perfusion: tachycardia, peripheral vasoconstriction, normal/mildly elevated blood pressure, mild/moderate hyperlactatemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Shock characteristics

A

Compensatory mechanisms become overwhelmed: symptomatic tachycardia, dyspnoea, restlessness, diaphoresis, metabolic acidosis, hypotension, oliguria, cool/clammy skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

At what reduction in arterial blood volume do clinical signs and symptoms of shock begin showing (hypovolemic)?

A

20-25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Progressive shock characteristics

A

Compensatory mechanisms completely overwhelmed, irreversible organ damage occurring. Signs and symptoms include: anuria, acute renal failure, acidemia, hypotension, hyperlatatemia, coma/death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

4 causes of shock

A

Cardiogenic, obstructive, hypovolemic, distributive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Most common cause of shock

A

Septic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Types of hypotension for shock

A

Absolute (SBP <90, MAP <65), relative (drop in SBP >40), orthostatic (drop in SBP >20 or DBP >10 with standing), or profound (vasopressor-dependent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Shock index

A

Shock index = heart rate/systolic blood pressure

SI>1 = bad

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pulse pressure in shock

A

Wide for distributive shock, narrow in other forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes of oliguria in shock

A

Shunting of renal blood flow, kidney injury, intravascular volume depletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cellular effects of shock

A
  1. Cell membrane ion pump dysfunction
  2. Intracellular oedema
  3. Leakage of intracellular contents into extracellular space
  4. Inadequate regulation of intracellular pH
  5. Acidosis
  6. Endothelial dysfunction
  7. Further stimulation of inflammatory and anti inflammatory cascades
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Endogenous causes of airway obstruction

A 
Airway oedema (anaphylaxis)
Mucus plug
Tongue displacement 
Infection (epiglottitis, croup)
Laryngospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Exogenous causes of airway obstruction

A

Foreign bodies

Trauma, burns, toxic gases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Foreign body airway obstruction epidemiology

A

80% of cases occur in children <3 years

Also common in elderly, people with dysphagia, altered conscious state, neurological problems (e.g. MND, Parkinson’s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Is FBAO more common on left or right bronchus? Why?

A

Right (less steep angle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Signs of effective coughing

A

Verbal response to questions, loud cough, able to breathe before coughing, fully responsive, stridor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Signs of ineffective coughing

A

Unable to vocalise, quite or silent cough, unable to breath, cyanosis, decreasing level of consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Differential diagnosis for FBAO

A

Croup, epiglottitis, anaphylaxis/angioedema, laryngeal spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pneumothorax definition

A

Gas in the pleural space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Pneumothorax categorisation

A

Spontaneous vs traumatic
Primary vs secondary (spontaneous)
Iatrogenic vs non-iatrogenic (traumatic)
Penetrating/open vs blunt/closed (non-iatrogenic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Pneumothorax epidemiology

A

Men more than women

1-37 per 100,000 per year

28
Q

Pneumothorax signs and symptoms - history

A

Dyspnoea, sudden onset, pleuritic chest pain, (trauma), (ventilated pts)

29
Q

Pneumothorax signs and symptoms - examination

A

Hypoxia, tachypnoea
Tracheal deviation - late sign, subcutaneous emphysema/“bubble wrap” skin, hyper-resonant to percussion, unequal air entry - equal air entry not exclusion criteria, tachycardia, distended neck veins/ increased JVP - late sign, displaced apex beat - late sign, decreased conscious state - late sign, (Marfanoid syndrome)

30
Q

Pneumothorax investigation

A

POCUS, decreasing EtCO2, hypotension not responding to fluids

31
Q

Tension pneumothorax signs

A

Increased respiratory distress in awake pt
Decreasing SpO2 to <92% despite O2
Decreasing conscious state
Poor perfusion or increasing HR +/- decreasing BP
Increasing peak inspiratory pressure (ventilator)/stiff bag
Decreasing EtCO2
Increasing jugular venous pressure
Tracheal shift

32
Q

Mnemonic for TPT decompression

A 
SMART
Second intercostal space
Mid-clavicular line
Above rib below
Right angle to chest
Towards body of vertebrae
33
Q

Vital signs for chest decompression (TPT)

A

GCS <10

BP <70

34
Q

What to do if pt is re-tensioning?

A

Flush cannula with 5-10mL of saline then (if ineffective) perform second decompression in close proximity on lateral side

35
Q

SVT definition

A

Technically includes any tachdysrhymias arising from above the level of the Bundle of His/above ventricles
Usually refers to AV nodal re-entry tachycardia (AVNRT) and sometimes AV re-entry tachycardia (AVRT)

36
Q

Paroxysmal SVT (pSVT)

A

SVT with abrupt onset and offset

37
Q

AVNRT characteristics and epidemiology

A

Most common cause of palpitations
Typically paroxysmal
Spontaneous or upon provocation (exertion, caffeine, alcohol, beta-agonists like salbutamol, sympathomimetics like amphetamines)
More common in women
May self resolve or continue indefinitely
Rarely life threatening

38
Q

AVNRT signs and symptoms

A

Presyncope or syncope (due to transient fall in blood pressure)
Chest pain
Dyspnoea
Anxiety

39
Q

AVNRT ECG features

A

P-waves absent or abnormal (retrograde p waves, p-wave inversion in leads II, III, aVF)
Narrow QRS complex (unless co-existing bundle branch block, accessory pathway or rate-related aberrant conduction)
Regular
Rate 140-280bpm

40
Q

AVRT characteristics

A

Anatomical re-entry due to accessory pathway bypassing AV node
Wolf-Parkinsons-White and Lown-Ganong-Levine are two conditions that can cause this
In WPW accessory pathway referred to as Bundle of Kent

41
Q

AVRT ECG features

A

PR interval short <120ms (signal is not delayed by AV node)
Delta wave
QRS prolongation >120ms
Rate >100

42
Q

Signs of decompensating SVT

A

Wet chest (APO)
Decreased perfusion/BP
Decreased conscious state
Ischaemic chest pain

43
Q

Alpha pathway of AV node

A

Slow depolarisation

Fast repolarisation

44
Q

Beta pathway of AV node

A

Fast depolarisation

Slow repolorisation

45
Q

Where are the main baroreceptors located?

A

Carotid sinus and aortic arch

46
Q

SVT signs and symptoms - history

A

Dyspnoea, choking sensation/abnormal sensation in throat, chest pain, palpitations, clammy/sweaty

47
Q

SVT signs and symptoms - examination

A

Clear chest/normal airway appearance, cool, pale, clammy, grey skin

48
Q

SVT signs and symptoms - investigation

A

ECG

49
Q

When to do valsalva manoeuvre

A

Stable AVNRT or AVRT
SBP >90
Standard valsava if manual handling or environmental concerns
Repeat 2x at 2 min intervals (max 3 attempts)

50
Q

4 phases of valsava

A
  1. Onset of straining (increases BP)
  2. Further increase in intrathoracic pressure (initially decreased BP then increases HR and BP)
  3. Strain release (decreases intrathoracic pressure which decreases BP)
  4. Increased BP activates baroreceptors leading to vagal tone outflow which decreases HR
51
Q

How does adenosine work?

A

Binds to type 1 (A1) receptors and coupled to Gi-proteins
Opens potassium channels (hyperpolarises cell) and inhibits calcium channels (prevents calcium entry into cell)
This means cell can’t reach threshold potential so it can’t depolarise resulting in a short period of asystole before the SA node takes over

52
Q

R-on-T phenomenon

A

Occurs when shock is delivered during relative refractory period (latter part of T-wave) which can induce VF

53
Q

First degree AV block

A

Prolonged PR interval >0.20 sec (sometimes so prolonged it goes into T-wave)
Usually caused by electrolyte imbalance
Not usually of much clinical significance

54
Q

2nd degree type 1 AV block (Wenckebach)

A

Progressive prolongation of PR interval culminating in non-conducting P-wave (group beating)
Can be caused by inferior MI, drugs like beta-blockers, calcium channel blockers, amiodarone, digoxin, increased vagal tone (athletes), myocarditis, following cardiac surgery
Usually benign and asymptomatic
Low risk of progressing to third degree

55
Q

Second degree type 2 (Hay)

A

Intermittent non-conducting p-waves without progressive prolongation of PR interval
Can be caused by anterior MI, hyperkalaemia, cardiac surgery, inflammatory conditions, drugs like beta-blockers, calcium channel blockers, digoxin, amidodarone
More likely to be associated with haemodynamic compromise, severe bradycardia and progression to 3rd degree

56
Q

Third degree/complete heart block

A

Severe bradycardia due to absence of AV conduction
AV dissociation - independent atrial and ventricular rates
Causes are same as for second degree type 2
Pts at high risk for ventricular standstill and sudden cardiac death

57
Q

Bradycardia categorisation

A

Regular or irregular

Narrow or wide complex

58
Q

Mild bradycardia vs marked bradycardia

A 
Mild = 50-60bpm
Marked = 30-45bpm
59
Q

Signs and symptoms of marked bradycardia

A 
Decreased BP (80-90mmHg) 
Decreased perfusion 
Cool, pale, clammy skin
Weak/absent pulse
Agitated, confused, light headed, unconscious 
Chest pain 
Dyspnoea
60
Q

Cardioprotective characteristic of bradycardia

A

Slower HR may be beneficial for ACS as it reduces workload/oxygen demand of the heart minimising extension of infarction and the potential to develop a life threatening rhythm

61
Q

Signs of unstable bradycardia

A

Less than adequate perfusion (including acute STEMI and ischaemic chest pain)
Profound bradycardia (<40bpm) and APO
Runs of VT or ventricular escape rhythms
HR <20bpm

62
Q

Cardiomyopathy definition

A

Myocardial disorder in which the heart muscle is structurally and functionally abnormal in the absence of coronary artery disease, hypertension, valvular disease, and congenital heart disease sufficient to explain the observed myocardial abnormality

63
Q

Bradycardia CPG care objectives

A

To increase HR where bradycardia is causing haemodynamic compromise, heart failure or life threatening arrhythmia

64
Q

Pulmonary oedema CPG care objectives

A

Nitrates treat underlying cause of cardiogenic APO and should be administered to all patients presenting in symptomatic cardiogenic APO unless contraindicated
CPAP is an appropriate treatment for respiratory failure associated with APO while the underlying cause is addressed. It may be required in patients unresponsive to nitrates or where respiratory failure is significant enough to require immediate treatment concurrent with nitrates
Furosemide is not an appropriate first line treatment in hypertensive patients with a sympathetically driven APO. Nitrates and CPAP (where required) should be the initial priority. Where the patient is normotensive or hypertension has been corrected with nitrates, furosemide may be considered

65
Q

Narrow complex tachycardia CPG care objectives

A

Rapid termination of life threatening arrhythmias and transport to a facility capable of definite care
Rapid transport to facilitate the treatment of the arrhythmia where treatment is not available in the prehospital environment
Early termination of stable SVT where possible, following ECG capture

66
Q

Shock CPG care objectives

A

To achieve a perfusion target appropriate to the patient’s condition

67
Q

Upper airway obstruction CPG care objectives

A

To identify and treat with the appropriate degree of urgency the potential airway obstruction indicated by stridor in adults

cardioresp (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions